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Curr Hypertens Rep. 2019 Apr 4;21(4):28. doi: 10.1007/s11906-019-0937-8.

Revisiting the Brain Renin-Angiotensin System-Focus on Novel Therapies.

Author information

1
Division of Pharmacology and Vascular Medicine, Department of Internal Medicine, Erasmus MC, Wytemaweg 80, 3015 CN, Rotterdam, The Netherlands.
2
AstraZeneca-Shenzhen University Joint Institute of Nephrology, Department of Physiology, Shenzhen University Health Science Center, Shenzhen University, Shenzhen, China.
3
Division of Pharmacology and Vascular Medicine, Department of Internal Medicine, Erasmus MC, Wytemaweg 80, 3015 CN, Rotterdam, The Netherlands. a.danser@erasmusmc.nl.

Abstract

PURPOSE OF REVIEW:

Although an independent brain renin-angiotensin system is often assumed to exist, evidence for this concept is weak. Most importantly, renin is lacking in the brain, and both brain angiotensinogen and angiotensin (Ang) II levels are exceptionally low. In fact, brain Ang II levels may well represent uptake of circulating Ang II via Ang II type 1 (AT1) receptors.

RECENT FINDINGS:

Nevertheless, novel drugs are now aimed at the brain RAS, i.e., aminopeptidase A inhibitors should block Ang III formation from Ang II, and hence diminish AT1 receptor stimulation by Ang III, while AT2 and Mas receptor agonists are reported to induce neuroprotection after stroke. The endogenous agonists of these receptors and their origin remain unknown. This review addresses the questions whether independent angiotensin generation truly occurs in the brain, what its relationship with the kidney is, and how centrally acting RAS blockers/agonists might work.

KEYWORDS:

AT2 receptor; Aminopeptidase A inhibitor; Angiotensinogen; Brain renin-angiotensin system; Kidney; Stroke; Sympathetic nervous system

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